Masteron as an antiestrogen

I know it might seem like I’m spending all day looking for new uses for old drugs, but in this case, nothing could be truer. Before I talk about how and why Masteron can be used as an antiestrogen, I will tell you how this idea came about and why I am talking about it. And yes, this technique works in real life, not just on paper (I’ve seen several athletes use it successfully).

Several years ago I read the first publications about Masteron (drostanolone propionate), understanding its real clinical uses: “Breast cancer reduction and as a hormonal treatment for breast cancer” … In short, Masteron is an anabolic-androgenic steroid used as an agent to prevent or inhibit the growth of estrogen-sensitive cancers.

So, in one of my studies on this molecule, I realized that gynecomastia, mastectomy and Masteron have something in common … in a way. You might think that studying andrology should have helped me notice this connection in the first place … however, I definitely needed more specific elements. I was then told that the UG lab had been doing research on Masteron for one year, trying to find the reason why it was always made with the propionate ester and whether it was also effective with the slow release ester. From there, another long period of research on this molecule began. In the end, Masteron was found to be equally effective with a sustained-release ester, and some “privileged” had the opportunity to try it with this particular ester before it was released on the PG market: the drug remains active for over 3 weeks; so it was mass produced and sold (it is still produced today and is one of the top selling products of this UG).

So, I continued my research on Masteron. After re-analyzing the connection, several things struck me.

The first thing that struck me was that Masteron was made for women!

Masteron is one of the few steroids that was made for women, not men, and most people / instructors tell women to avoid it! And another thing that I noticed right away is that it is used to treat breast cancer.
In particular, it is used to treat estrogen-dependent breast cancer . For example, Nolvadex is also used clinically for the same purpose, such as Arimidex, Femara, Aromasin (a steroid aromatase inhibitor), and Teslac (a steroid, technically). But it is interesting to note that Teslac is actually a steroid and Aromasin is also a steroid aromatase inhibitor.

So why can’t a “real” steroid do the same job as preventing breast cancer?

The answer is:

To understand why Masteron can be used as an antiestrogen, we first need to know that it is a DHT derivative.

Why is this important?

This is important because DHT is able to directly suppress estrogenic activity in tissues. It probably does this by acting as a competitive estrogen receptor antagonist or by decreasing estrogen receptor binding. In both cases, it has several putative mechanisms of action in certain tissues, and it has also been suggested that DHT effectively suppresses the effects of estrogen not only by inhibiting estrogen receptor activity, but also by lowering circulating estrogen levels by inhibiting testosterone / AAS aromatization. This means that in very simple terms, estrogen activity is kept low by decreasing its activity. This means that you can take steroids that convert to estrogens (aromatized steroids) without worrying about estrogens going over, causing water retention, fat accumulation in the female model, etc.
In addition, this could mean that the antiestrogenic effect of DHT is mediated by the androgen receptor mechanism. In fact, DHT has been shown to prevent estrogen-dependent increases in the progesterone receptor in human breast cancer cells. And, not to be superfluous, but important to remember, almost all of the anti-estrogens we use to control gynecomastia and water retention are also used to treat breast cancer. So, we now know that some androgens are capable of inhibiting both the activity of the aromatase enzyme, preventing the conversion of aromatized AAS to estrogens, and inhibiting the activity of estrogen receptors in tissues, but they do not significantly affect the basal concentration of these receptors. Dihydrotestosterone (DHT) demonstrates a high degree of estrogen inhibition in human breast cancer cells. But not only DHT can do this, its metabolites inhibit aromatization itself, DHT, androsterone and 5alpha-androstanedione are powerful inhibitors of the formation of estrone from androstenedione. In fact, it is so effective in lowering estrogen levels that DHT transdermal gel applied to the affected area has been used to treat gynecomastia. DHT is just as effective as antiestrogens that it has also been used to increase height in children with growth deficits and since this increase was found to be unrelated to the effects of GH It has been strongly suggested that the anti-estrogenic effects of DHT are a mechanism by which growth can be increased in subjects affected by this pathology. Of course, I don’t need to tell you that DHT is structurally incapable of converting to estrogen.

So this all shows us that DHT certainly has a positive effect on estrogen control: but what about Masteron? Can it be effectively used for this purpose? Well, let’s take a close look at Masteron and see the differences it presents in comparison to DHT. But before doing that, I think a short explanation of DHT is needed. Don’t worry, I’ll get it done as soon as possible.

Dihydrotestosterone (DHT) [full name: 5α-Dihydrotestosterone, abbreviated 5α-DHT; INN: androstanolone] is a biologically active metabolite of the testosterone hormone, formed mainly in the prostate gland, testes, hair follicles and adrenal glands under the action of the enzyme 5α-reductase with a decrease in the double bond between the 4th and 5th carbon atoms. This process is called (obviously) 5-alpha reduction.

testosterone-diidrotestosterone differenza

So now we know how testosterone is converted to dihydrotestosterone. And it would be easier if this were the only thing that happens to our good old friend Testosterone, because, as you may already know, DHT is a much more powerful androgen than the molecule it comes from. Unfortunately, this is not the end of the story, because DHT is largely inactivated by the enzyme 3-alpha hydroxyysteroid dehydrogenase (3bHSD), which is mainly present in skeletal muscle.

For our purposes, we are only interested in understanding the specific action of this enzyme.
It can convert a steroid with a ketone group at position 3 of a steroid to one with a hydroxyl group at the same position by converting so DHT to androstanediol. This conversion is, in part, the only reason DHT has not been shown to be a very effective anabolic, and androstanediol is not known to be very anabolic. If you observe the molecular structure after DHT conversion, you will notice that “O” (oxygen) has been replaced with “HO” (hydrogen + oxygen) in the third position.

androstanediol

3bHSD is present throughout the body (like 5a-R, for the most part), but is found in high concentrations in the scalp and prostate gland, and it is also possible that its effects on DHT exacerbate baldness. Man. In addition, it is worth noting that DHT is an androgen responsible for the development of the external genitalia. This is probably the reason why women experience temporary clitoral hypertrophy when they use their frequently recommended steroids (Primobolan, Anavar, Winstrol, etc.) in excessive doses.
I found it really interesting that the most commonly recommended steroids Are those that most commonly cause clitoral enlargement and other possible androgenic effects. But the good news, in my experience with female athletes, is that the first effect is welcome. Topical DHT can also be used to treat Microphalia (very small genitals) in men.

Now you know what DHT is, where it comes from, what it can do, and why it is not a particularly strong anabolic when used alone.

Now let’s take a closer look at Masteron and how it differs from its parent molecule, DHT.

Drostanolone (MASTERON)

drostanolone-propionato To get DROSTANOLONE (MASTERON) 2a-methyl-dihydro-testosterone, a methyl group is added to dihydrotestosterone at C-2, thus obtaining an increase in resistance to the 3a-HSD keto group C-3, but not improving oral bioavailability over DHT. Slightly improves biological activity due to slightly lower affinity for SHBG. In Masteron, which is a reduced 5-alpha compound, there is no aromatization. Indeed, as mentioned above, it has antiestrogenic activity similar to that of mesterolone (Proviron), quantified similarly to that of Nolvadex, which, together with its strong affinity for androgen fat receptors (which stimulate lipolysis), has long made it a typical AAS for pre-competition … The official anabolic androgenic ratio is 25/40 – 62/130.

I know it might seem like I’m spending all day looking for new uses for old drugs, but in this case, nothing could be truer. Before talking about how and why Masteron can be used as an antiestrogen, I will talk about how this idea was born and why I am talking about it. And yes, this technique works in real life, not just on paper (I’ve seen several athletes use it successfully).

Several years ago I read the first publications about Masteron (drostanolone propionate), understanding its real clinical uses: “Breast cancer reduction and as a hormonal treatment for breast cancer” … In short, Masteron is an anabolic-androgenic steroid used as a means to prevent or inhibit the growth of estrogen-sensitive cancers.

So, in one of my studies on this molecule, I realized that gynecomastia, mastectomy and Masteron have something in common … in a way. You might think that studying andrology should have helped me notice this connection in the first place … however, I definitely needed more specific elements. I was then told that a yearlong UG lab did research on Masteron looking for a reason why it was always made with propionate ester and whether it would be as effective with slow release ester as well. From there, another long period of research on this molecule began. In the end, Masteron was found to be equally effective with a sustained-release ester, and some “privileged” had the opportunity to try it with this particular ester before it was released on the PG market: the drug remains active for over 3 weeks; so it was mass produced and sold (it is still in production today and is one of the best selling products of this UG)

So, I continued my research on Masteron. After re-analyzing the connection, several things struck me.

The first thing that struck me was that Masteron was made for women!

Masteron is one of the few steroids that was made for women, not men, and most people / instructors tell women to avoid it! And another thing I noticed right away is that it is used to treat breast cancer.
In particular, it is used to treat estrogen-dependent breast cancer . For example, Nolvadex is also used clinically for the same purpose, such as Arimidex, Femara, Aromasin (a steroid aromatase inhibitor), and Teslac (a steroid, technically). But it is interesting to note that Teslac is actually a steroid and Aromasin is also a steroid aromatase inhibitor.

So why can’t a “real” steroid do the same job as preventing breast cancer?

The answer is:

To understand why Masteron can be used as an antiestrogen, we first need to know that it is a DHT derivative.

Why is this important?

This is important because DHT is able to directly suppress the activity of estrogen in tissues. It probably does this by acting as a competitive estrogen receptor antagonist or by decreasing estrogen receptor binding. In both cases, it has several putative mechanisms of action in some tissues. It has also been suggested that DHT actually suppresses the action of estrogen not only by inhibiting estrogen receptor activity, but also by decreasing circulating estrogen levels by inhibiting testosterone / AAS aromatization.This means that in very simple terms, estrogen activity is kept low by decrease in its activity. This means that you can take steroids that convert to estrogens (aromatized steroids) without worrying about estrogens going over, causing water retention, fat accumulation in the female model, etc.
In addition, this could mean that the antiestrogenic effect of DHT is mediated by the androgen receptor mechanism. In fact, DHT has been shown to prevent estrogen-dependent increases in the progesterone receptor in human breast cancer cells. And, not to be superfluous, but important to remember, almost all of the anti-estrogens we use to control gynecomastia and water retention are also used to treat breast cancer. So, we now know that some androgens are capable of inhibiting both the activity of the aromatase enzyme, preventing the conversion of aromatized AAS to estrogens, and inhibiting the activity of estrogen receptors in tissues, but they do not significantly affect the basal concentration of these receptors. Dihydrotestosterone (DHT) demonstrates a high degree of estrogen inhibition in human breast cancer cells. But not only DHT can do this, its metabolites inhibit aromatization itself, DHT, androsterone and 5alpha-androstanedione are powerful inhibitors of the formation of estrone from androstenedione. In fact, it is so effective in lowering estrogen that DHT transdermal gel applied to the affected area has been used to treat gynecomastia, DHT is as effective as antiestrogens that it has also been used to increase growth in children with deficiencies growth, and since this increase was found to be unrelated to the effects of GH It has been strongly suggested that the anti-estrogenic effects of DHT are a mechanism by which growth can be increased in subjects affected by this pathology. Of course, I don’t need to tell you that DHT is structurally incapable of converting to estrogen.

So this all shows us that DHT certainly has a positive effect on estrogen control: but what about Masteron? Can it be effectively used for this purpose? Well, let’s take a close look at Masteron and see the differences it presents in comparison to DHT. But before doing that, I think a short explanation of DHT is needed. Don’t worry, I’ll get it done as soon as possible.

Dihydrotestosterone (DHT) [full name: 5α-Dihydrotestosterone, abbreviated 5α-DHT; INN: androstanolone] is a biologically active metabolite of the testosterone hormone, formed mainly in the prostate gland, testes, hair follicles and adrenal glands under the action of the enzyme 5α-reductase with a decrease in the double bond between the 4th and 5th carbon atoms. This process is called (obviously) 5-alpha reduction.

testosterone-diidrotestosterone differenza

So now we know how testosterone is converted to dihydrotestosterone. And it would be easier if it was the only thing that happens to our good old friend Testosterone, because as you may already know, DHT is a much more powerful androgen than the molecule it comes from. But, Unfortunately, this is not the end of the story, because DHT is largely inactivated by the enzyme 3-alpha hydroxyysteroid dehydrogenase (3bHSD), which is mainly present in skeletal muscle.

For our purposes, we are only interested in understanding the specific action of this enzyme.
It can convert a steroid with a ketone group at position 3 of a steroid to one with a hydroxyl group at the same position by converting so DHT to androstanediol. This conversion is, in part, the only reason DHT has not been proven to be a very effective anabolic, such as androstanediol, which is not known to be very anabolic. If you observe the molecular structure after DHT conversion, you will notice that “O” (oxygen) has been replaced with “HO” (hydrogen + oxygen) in the third position.

androstanediol

3bHSD is present throughout the body (like 5a-R, for the most part), but is found in high concentrations in the scalp and prostate gland, and it is also possible that its effects on DHT exacerbate baldness. Man. In addition, it is worth noting that DHT is an androgen responsible for the development of the external genitalia. This is probably the reason why women experience temporary clitoral hypertrophy when they use frequently recommended steroids (Primobolan, Anavar, Winstrol, etc.) in excessive doses.
I found it really interesting that the most commonly recommended steroids are the ones that most commonly cause clitoris enlargement and other possible androgenic effects. But the positive thing in my experience with female athletes is that the first effect is welcome. Topical DHT can also be used to treat Microphalia (very small genitals) in men.

Now you know what DHT is, where it comes from, what it can do, and why it is not a particularly strong anabolic when used alone.

Now let’s take a closer look at Masteron and how it differs from its parent molecule, DHT.

Drostanolone (MASTERON)

drostanolone-propionato To get DROSTANOLONE (MASTERON) 2a-methyl-dihydro-testosterone, a methyl group is added to dihydrotestosterone at C-2, thus obtaining an increase in resistance to the 3a-HSD keto group C-3, but not improving oral bioavailability over DHT. Slightly improves biological activity due to slightly lower affinity for SHBG. In Masteron, which is a reduced 5-alpha compound, there is no aromatization. Indeed, as mentioned above, it has antiestrogenic activity similar to that of mesterolone (Proviron), quantified similarly to that of Nolvadex, which, together with its strong affinity for androgen fat receptors (which stimulate lipolysis), has long made it a typical AAS for pre-competition … The official anabolic androgenic ratio is 25/40 – 62/130.

This 2-alpha methyl change makes the compound much more anabolic, even though it is still only 60% anabolic on average compared to testosterone and the fourth androgen.Of course, these ratings do not make it the most potent anabolic in the world. but its anti-estrogenic action (anti-aromatase action) plus its ability to increase aggression and lipolysis make it a good pre-race adjunct. There is also a widespread belief that Masteron will not benefit the user if they are not in a physical condition in which the percentage of body fat is very low. It’s not like that at all. It doesn’t matter what percentage of body fat you have, if you want Masteron’s pleasing anti-estrogenic effects, as well as an increase in aggression and strength in the gym (the former and the latter are known as “non-genomic effects”). “)

And are the result of strong effects stimulated by the interaction of Masteron with the central nervous system, which is a very common feature of DHT-derived steroids. Basically, if your body fat percentage is high, but you are taking something to increase aggression and that it has an anti-estrogenic effect (for example, Halotestin and Arimidex), you certainly should not expect you to get huge and pulled, but this is not means the use is useless. It’s the same with Masteron. Now, what if an already fat-reduced athlete adds Arimidex and Halotestin to the cycle before the race? the best aesthetic and muscular aspect will be obtained.

This is exactly what happens if you add Masteron to the loop before the competition. It is not that the athlete must have an arbitrary percentage of body fat in order to obtain this type of results, but that he must be in a physical condition in which the percentage of body fat is low enough to “see” these results. Again, if a given athlete has a high percentage of body fat and is taking Halotestin and Arimidex, they will not be using it for aesthetic purposes. Think of Masteron in these terms, even if it does not work as well for aggression as Halotestin and it will not be as good at fighting estrogen as Arimidex. Compared to these two compounds, Masteron is likely to have several effects (on appearance and strength). But if you’re looking to make a low dose cycle with as few compounds as possible, a simple mixture of testosterone (propionate) and masteron in a cycle might be exactly what you’re looking for. Personally, I have seen a similar cycle used by different athletes: they mixed 100 mg of testosterone propionate and 100 mg of masteron on different days or every day throughout the training period.
Usually men use Masteron in doses of 300-500 mg per week. Masteron has a high binding rate with SHBG and albumin. Since these two hormone-binding proteins prevent AAS from binding to their receptor, one might think that this is not a good thing.
Masteron is 3-5 times more active than testosterone at binding to the receptor, so some of the legacy circulating in blood flow, goes a long way, binding to its target receptor and carrying out its antiestrogenic activity. Since the molecule binds a high percentage of SHBG and albumin, any other AAS administered with it remains unbound and therefore active, free, longer lasting, and is capable of eliciting a greater androgenic-anabolic response.

But is Masteron really considered an effective antiestrogen?

Yes .

From 1968 to 1972, a significant study was conducted on Masteron, in a group of premenopausal women with breast cancer. About a third responded well to Masteron, evidently due to its antiestrogenic effects, although not comparable to those of arimidex, letrozole or aromasin. Unless you cycle with a lot of flavored steroids, this molecule is a very good choice to add to your cycle. If, on the other hand, you are taking large amounts of these flavoring compounds, then it is recommended that you use a traditional antiestrogen as your cycle compound. But if you’re taking a weekly amount under a gram of flavored steroids, Masteron is likely to be the only anti-estrogen needed. This report is based on my experiences with the athletes I interviewed.

MASTERON AND USE IN WOMEN

Now I would like to briefly discuss the use of Masteron in women. Masteron was designed for women and that should be clear by now, right? If you paid attention up to this point, you already know that Masteron is indicated for women and is a DHT derivative, like most other steroids commonly used and recommended for female athletes (Primobolan, Anavar, Winstrol, etc.). … they are all DHT derivatives). And another notable fact is that Masteron has a lower androgenic value than almost all other steroids commonly recommended and used by female athletes. Anavar has an androgenic value of 24 compared to testosterone, and Masteron has an androgenic value of 25 always compared to testosterone, expressed as a percentage (this means 24% and 25% respectively).

Basically, Masteron works as hormone therapy for breast cancer and has proven to be useful and safe for use in women of all ages, although it may seem less effective than other possible treatments used in postmenopausal patients. Therefore, it is very safe for women, Masteron is certainly no less safe than Anavar or Primobolan for women, provided that it is used with a certain intelligence.
My recommendations for women for using this compound can start at a dosage of 10-25 mg every three days, and increase doses if no side effects are observed. At these dosages, side effects are unlikely to occur, and it can easily be said that there will be no dramatic side effects when using 20mg given every other day.
Here is a whole new look at an old molecule (Masteron) is useful as an antiestrogen and also anabolic steroid that can certainly be used safely by men and women.

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